ﺑﺎﺯﮔﺸﺖ ﺑﻪ ﺻﻔﺤﻪ ﻗﺒﻠﯽ
خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده : 3 مورد
نسخه الکترونیک
medimedia.ir

Treatment and prevention of streptococcal pharyngitis in adults and children

Treatment and prevention of streptococcal pharyngitis in adults and children
Literature review current through: Jan 2024.
This topic last updated: Jan 23, 2024.

INTRODUCTION — Group A Streptococcus (GAS), or Streptococcus pyogenes, is the leading bacterial cause of tonsillopharyngitis in adults and children worldwide. GAS is one of the few causes of tonsillopharyngitis or pharyngitis for which antibiotic treatment is recommended.

The treatment and prevention of group A streptococcal tonsillopharyngitis is reviewed here. The clinical features and diagnostic evaluation of patients with tonsillopharyngitis are discussed separately. (See "Group A streptococcal tonsillopharyngitis in children and adolescents: Clinical features and diagnosis" and "Evaluation of acute pharyngitis in adults".)

DEFINITIONS — Group A Streptococcus (GAS) can cause symptomatic infection or can colonize the oropharynx.

Active infection refers to symptomatic infection caused by GAS.

Persistent infection refers to symptomatic infection caused by GAS that does not resolve after appropriate antibiotic treatment. This is synonymous with treatment failure.

Recurrent infection refers to a new symptomatic infection with GAS that occurs after appropriate antibiotic treatment. Recurrent infection can be caused by the same GAS serotype that caused the initial infection or by a different serotype. Recurrent infections most often occur among members of the same household or in other settings such as schools or daycare centers where close contact facilitates GAS transmission [1].

Chronic carriage refers to asymptomatic colonization or the persistent presence of GAS in the oropharynx in the absence of symptoms or host immune response. The prevalence of chronic carriage has not been comprehensively studied, but reported rates are about 4 to 5 percent in healthy adults [2] and range from about 2 to 20 percent in children [2-9]. Carriage can persist for months to years [8,10].

Distinguishing among these states is important. In general, only patients with symptomatic GAS infection require treatment. Exceptions include patients with a history of acute rheumatic fever, and chronic GAS carriers during outbreaks of acute rheumatic fever and/or poststreptococcal glomerulonephritis, or when GAS infections are recurring in households or other close-contact settings.

GOALS OF TREATMENT — The goal of antibiotic therapy for streptococcal pharyngitis is multifold and includes:

Reducing symptom severity and duration

Prevention of acute complications, such as otitis media, peritonsillar abscesses, or other invasive infections

Prevention of delayed complications or immune sequelae, particularly acute rheumatic fever

Prevention of spread to others

Symptom reduction — Antibiotic treatment has been shown to reduce symptom severity and hasten the rate of recovery in patients with streptococcal pharyngitis [11,12]. However, even without antibiotic therapy, symptoms typically resolve in about three to five days for most patients [13], making the prevention of complications a key goal of care.

Prevention of complications — Complications of streptococcal pharyngitis can result from extension of infection beyond the oropharynx, termed suppurative complications, or as immune phenomena, termed nonsuppurative complications. Suppurative complications of GAS pharyngitis include otitis media, peritonsillar cellulitis or abscess, sinusitis, meningitis, bacteremia, and necrotizing fasciitis. Nonsuppurative complications of GAS pharyngitis include acute rheumatic fever, poststreptococcal glomerulonephritis, and reactive arthritis. The spectrum of complications associated with streptococcal pharyngitis is discussed in detail separately. (See "Complications of streptococcal tonsillopharyngitis".)

Suppurative complications — Rates of otitis media and peritonsillar abscesses are each reduced with antibiotic use. In a large meta-analysis of randomized trials comparing antibiotics to placebo in adults and children with streptococcal pharyngitis, antibiotics reduced the incidence of acute otitis media within 14 days (0.47 versus 2.0 percent; risk ratio [RR] 0.30, 95% CI 0.15-0.58) and peritonsillar abscess at two months (0.24 versus 2.3 percent; RR 0.15, 95% CI 0.05-0.47) [11]. Reduction in the rates of acute sinusitis were also observed but did not reach statistical significance. The effect on less common but severe suppurative complications including bacteremia and necrotizing fasciitis has not been studied, though it is reasonable to surmise that antibiotics would have a protective effect.

Nonsuppurative complications

Acute rheumatic fever — The prevention of acute rheumatic fever is one of the main indications for antibiotic treatment of streptococcal pharyngitis. Acute rheumatic fever and rheumatic heart disease are important causes of cardiovascular death worldwide [14,15]. In a meta-analysis of 14 randomized trials comparing penicillin with placebo in over 8000 adults and children with sore throat, penicillin decreased the risk of rheumatic fever by about two-thirds [11]. The absolute risk reduction is likely highest in children aged 5 to 15 residing in developing nations, where incidence of rheumatic fever peaks [15,16]. Additional detail on acute rheumatic fever is provided separately. (See "Acute rheumatic fever: Epidemiology and pathogenesis" and "Acute rheumatic fever: Clinical manifestations and diagnosis" and "Acute rheumatic fever: Treatment and prevention".)

Other nonsuppurative complications — Data on the benefits of antibiotics in preventing other nonsuppurative complications are limited. Antibiotics probably prevent poststreptococcal glomerulonephritis based on a meta-analysis of 10 randomized trials comparing antibiotics with placebo in adults and children with sore throat, though there were too few cases in these trials to conclude this with certainty [11]. The effect of antibiotics on other nonsuppurative complications such as poststreptococcal arthritis and pediatric autoimmune neuropsychiatric disorder associated with group A streptococci (PANDAS) is not well studied. Additional details on these complications are provided separately. (See "Poststreptococcal glomerulonephritis" and "Complications of streptococcal tonsillopharyngitis".)

Prevention of transmission — GAS can spread among close contacts, leading to clusters of cases and recurrent infections in households or other close-contact settings. The rate of GAS transmission from an infectious case to close contacts is estimated to be between 5 and 50 percent [17-19]. Although no studies have directly evaluated the effect of antibiotic treatment on transmission, antibiotic use appears to eliminate GAS from the oropharynx in about 80 to 90 percent of cases after 24 hours of therapy [20,21]. When untreated, historic epidemiologic data suggest approximately 50 percent of patients with streptococcal pharyngitis will continue to harbor GAS in the oropharynx three to four weeks after symptom onset [13,22].

WHOM TO TREAT — We recommend antibiotic treatment for any patient with symptomatic pharyngitis or tonsillopharyngitis who has a positive microbiologic test (ie, nucleic acid amplification test [NAAT], rapid antigen test, or culture) for group A Streptococcus (GAS) (algorithm 1). (See "Evaluation of acute pharyngitis in adults", section on 'Evaluation' and "Group A streptococcal tonsillopharyngitis in children and adolescents: Clinical features and diagnosis".)

Empiric treatment is generally not recommended, as the clinical features of GAS pharyngitis and nonstreptococcal pharyngitis broadly overlap (figure 1) [23,24]. Short delays in therapy (eg, while awaiting culture results) have not been associated with increased rates of complications such as acute rheumatic fever [22]. However, whether such delays effect rates of other complications (eg, development of peritonsillar abscess) is not known. If clinical suspicion for GAS pharyngitis is high and testing results cannot be obtained rapidly, it is reasonable to start antibiotic treatment while test results are pending [25]. If testing does not confirm the diagnosis, antibiotics should be discontinued.

Antibiotic treatment is not recommended for asymptomatic chronic GAS carriers or for GAS carriers who have superimposed viral infections [23,24,26]. (See 'Chronic GAS carriers' below.)

TREATMENT OF INITIAL EPISODES — Antibiotic treatment is the mainstay of care. (Related Pathway(s): Streptococcal pharyngitis in adults: Treatment.)

Supportive care measures such as nonsteroidal anti-inflammatory drugs (NSAIDs) or acetaminophen may be administered to relieve fever and pain.

Antibiotic treatment — The antibiotic treatment recommendations presented below are largely consistent with recommendations from the Infectious Diseases Society of America, the American Heart Association, and the American Academy of Pediatrics (algorithm 2) [23,26-28]. Guidelines from other regions vary [29-31].

Penicillin — Penicillin is the treatment of choice for group A Streptococcus (GAS) pharyngitis due to its efficacy, safety, narrow spectrum, and low cost. Resistance to penicillin among clinical GAS isolates has not been documented. Penicillin is the only antibiotic that has been studied and shown to reduce rates of acute rheumatic fever [11]. Dosing and duration of therapy are outlined in the tables (table 1 and table 2).

For most adult patients, we use oral penicillin V 500 mg two to three times daily for 10 days. Oral amoxicillin is also a reasonable option.

For most children, we use either oral penicillin V or amoxicillin. Amoxicillin is often preferred for young children because the taste of the amoxicillin suspension is more palatable than that of penicillin. Amoxicillin can also be given once daily. In several randomized trials, standard-dose and once-daily dosing of amoxicillin appeared to have equivalent efficacy as oral penicillin [32-36].

For patients with a history of acute rheumatic fever who are not receiving antibiotic prophylaxis, we select among oral penicillin V, oral amoxicillin, or a single dose of intramuscular (IM) penicillin G benzathine. Because adherence is critical for patients with a history of acute rheumatic fever, we base our choice on patient values and preferences. While IM benzathine penicillin can be given as a single dose, the drug is expensive in some regions, frequently unavailable, and causes injection site pain. In contrast, oral options are readily available but carry the risk of incomplete adherence. (See "Acute rheumatic fever: Treatment and prevention".)

The duration of therapy for oral penicillin or amoxicillin is 10 days. Although symptoms typically improve within the first few days of treatment [13,37,38], treating for 10 days appears to enhance the rate of GAS eradication from the oropharynx when compared with 5 or 7 days [3,23,39-41]. One randomized trial directly compared a 5-day course of penicillin V 800 mg four times daily with a 10-day course of penicillin V dosed at 1000 mg three times daily in 433 patients (age ≥6) with microbiologically confirmed streptococcal pharyngitis [42]. Clinical cure rates were similar between groups (89.6 versus 93.8 percent; difference -4.2, 95% CI -9.9 to 1.5); however, wide confidence intervals suggest that treatment differences may become apparent with a larger sample size. In addition, bacterial eradication rates were lower in the 5-day treatment group (80.4 versus 90.7 percent). Complication rates were also similar between groups but their overall frequency was low (1 percent). Because complications, particularly immune sequelae, are likely related to the presence of GAS in oropharynx and can be severe, treating with a 10-day course seems prudent.

IM penicillin appears to be more effective than oral penicillin at eradication of GAS from the oropharynx [43] and has been most well studied for the prevention of acute rheumatic fever [11]. However, as noted above, IM penicillin is expensive in some regions and not always available. Thus, for patients with a history of acute rheumatic fever (who are high risk for cardiac complications compared with those without this history), we discuss the risk and benefits of its use on an individual basis.

Alternatives to penicillin — Cephalosporins, clindamycin, and macrolides are alternatives for patients who are allergic to penicillin or who cannot otherwise tolerate penicillin. Dosing and duration of therapy are outlined in the tables (table 1 and table 2).

Selection of an agent depends on the type of allergy, local antibiotic resistance rates, and patient values and preferences (table 3 and algorithm 2).

The approach to antibiotic selection for patients with penicillin allergy varies among experts:

For patients with mild, non-IgE-mediated reactions to penicillin (eg, maculopapular rash beginning days into therapy), the author and editors of this topic generally select a first-generation cephalosporin such as cephalexin because of its narrow spectrum and the low likelihood of cross-reactivity.

For patients with mild, possibly IgE-mediated reactions (eg, urticaria or angioedema but not anaphylaxis), they use a second- or third-generation cephalosporin with a side chain that is dissimilar to penicillin, such as cefuroxime, cefdinir, or cefpodoxime.

When using an oral cephalosporin, we generally treat for 10 days. A five-day treatment course with cefdinir or cefpodoxime is also acceptable. These shorter treatment courses are US Food and Drug Administration approved and, in randomized trials, had similar clinical and microbiologic efficacy as 10-day courses of oral penicillin [44-47].

For patients with a history of severe angioedema and/or anaphylaxis or with serious delayed reactions or for patients who cannot take cephalosporins, we generally use a macrolide, such as azithromycin. A major advantage of azithromycin is that it can be given for a three- or five-day course due to its extended half-life [48].

A key consideration when using a macrolide is potential drug resistance. Macrolide resistance rates are growing and vary with geography [49-54]. Generally, higher macrolide resistance rates have been observed in Asia and Europe when compared with the United States. Clinicians should take into account local resistance patterns or consult local antibiograms when prescribing macrolides, if possible.

For patients with known or suspected macrolide-resistant GAS who cannot tolerate cephalosporins, we treat with a 10-day course of clindamycin.

The above approach is generally consistent with recommendations from both the American Academy of Pediatrics and the Infectious Diseases Society of America [23,28].

Other experts, including UpToDate allergy specialists, prefer to perform a test-dose procedure before prescribing cephalosporins to patients with penicillin allergies (algorithm 3). Because this is generally not feasible in the outpatient clinic, a more conservative approach to treatment is an option for patients with mild, non-IgE-mediated reactions or IgE-mediated reactions:

For patients with mild, non-IgE-mediated reactions, a third-generation cephalosporin, such as cefpodoxime or cefdinir, is selected.

For patients with any possible IgE-mediated reactions (including anaphylaxis), an alternative to cephalosporins such as a macrolide or clindamycin is selected.

The approach to the management of patients with penicillin allergy is reviewed separately. (See "Choice of antibiotics in penicillin-allergic hospitalized patients".)

No clinically relevant differences in symptom resolution were detected in a meta-analysis of 19 randomized trials comparing cephalosporins, macrolides, or clindamycin with either penicillin or amoxicillin in over 5000 adults or children with GAS [55]. While the incidence of clinical relapse was lower when comparing treatment with cephalosporins versus penicillins (26 versus 46 per 1000 patients; odds ratio 0.55, 95% CI 0.30-0.99), broad use of cephalosporins may promote antimicrobial resistance and are generally more costly than penicillins. No trial has evaluated the use of alternatives to penicillin for the prevention of acute rheumatic fever; thus, penicillin remains the treatment of choice when feasible.

Tetracyclines, sulfonamides, and fluoroquinolones should not be used for treatment of streptococcal pharyngitis due to the high prevalence of resistance [49-54], potential for clinical failure, and/or high side-effect profile [56].

Adjunctive treatment — We offer supportive care (rest, adequate fluid intake, avoidance of respiratory irritants, soft diet) to all patients and systemic agents such as NSAIDs or acetaminophen for patients who desire medication for fever or pain control. We avoid using systemic glucocorticoids for symptom relief because antibiotics and systemic analgesics are generally effective, and the addition of systemic glucocorticoids increases the likelihood of adverse events.

Symptomatic treatment for sore throat is discussed in detail separately. (See "Acute pharyngitis in children and adolescents: Symptomatic treatment" and "Symptomatic treatment of acute pharyngitis in adults".)

RESPONSE TO THERAPY

Resolution of symptoms — Fever and constitutional symptoms typically resolve within one to three days of starting treatment [13,57-61]. Follow-up visits are not needed for most patients.

Most patients can return to work or school after completing one full day of treatment, provided they are afebrile and otherwise well. This recommendation is based on a small cohort study in children that showed that about 80 percent of patients with culture-proven group A streptococcal (GAS) pharyngitis clear the organism from the oropharynx within 24 hours of starting therapy [20]. A second cohort study evaluating 111 children with pharyngitis and a positive rapid antigen detection test (RADT) showed that 91 percent of patients treated with amoxicillin by 5:00 PM on the day of therapy had negative follow-up RADTs the following morning [21].

Indications for test of cure — For patients who are asymptomatic at the end of a course of antibiotic therapy, a test of cure is typically not needed [62]. We generally perform a test of cure (culture or RADT) in the following patients, who are at risk for complications, recurrent infection, or spreading infection to others:

Patients with a history of acute rheumatic fever

Patients who acquired infection during an outbreak of acute rheumatic fever or poststreptococcal glomerulonephritis

Patients who acquired infection during a cluster of cases in their household or other close-contact setting

For patients who test positive in these circumstances, we repeat a full 10-day course of therapy. We usually select an antibiotic that has greater beta-lactamase stability than the one used for the initial treatment course. As examples, if penicillin was used for initial treatment, we use either amoxicillin-clavulanate or a first-generation cephalosporin; if a first-generation cephalosporin was used, we select a later-generation cephalosporin. The rationale for this strategy is based on clinical data that suggest relapse rates may be lower with cephalosporin use, as well as scientific observations that antibiotics with greater beta-lactamase activity may be more effective in eradicating GAS from the oropharynx. (See 'Antibiotic treatment' above.)

We do not treat patients who are asymptomatic following an appropriate course of therapy who test positive but lacked an appropriate indication for a test of cure. The patients are likely chronic carriers. (See 'Definitions' above.)

Persistent or recurrent symptoms

Evaluation — For patients who have persistent or recurrent symptoms consistent with GAS pharyngitis after completing a course of antibiotic therapy, we generally repeat testing for GAS. Because chronic GAS carriage can occur after antibiotic therapy [2-9], we generally avoid testing in patients whose symptoms are highly consistent with viral pharyngitis (eg, sore throat accompanied by cough, conjunctivitis, or rhinorrhea) or other etiology. For patients with persistent or recurrent symptoms consistent with GAS pharyngitis, a positive test result should raise suspicion for any of the following:

Nonadherence with the prescribed antimicrobial regimen

Recurrent infection, which refers to new infection with the initial infecting strain or a new strain

Persistent infection, also termed treatment failure

Infection with a different pathogen superimposed on chronic GAS carriage

Presence of a suppurative complication, such as a peritonsillar abscess

Distinguishing among these states is typically based on epidemiologic and clinical history, which can be challenging as symptoms overlap and GAS testing can be positive in all.

Suspicion for recurrent infection should be raised when clusters of GAS infections are occurring within the patient's household, school, workplace, or other close-contact setting. Symptoms associated with recurrent infection with the same serotype may be milder than with the initial infection [63]. Persistent infection is rare but most often occurs in children, particularly those under age 5 [64]. Initial antibiotic choice may also influence the likelihood of recurrent or persistent infection. Selection of an antibiotic to which there is potential GAS resistance, such as a macrolide or clindamycin, increases the likelihood of treatment failure. Additionally, some studies suggest that cephalosporins may be more effective than penicillin for preventing relapse [65].

The presence of persistent or recurrent symptoms should also raise suspicion for an alternate initial diagnosis or new infection with a different pathogen in a chronic GAS carrier. For patients with repeated episodes of pharyngitis, culturing for GAS when patients are between episodes may help distinguish chronic carriage from active infection. A positive culture in an asymptomatic patients suggests that the patient is a carrier and that symptoms are due to an alternate cause (table 4 and table 5). Additional details on the evaluation of acute pharyngitis are discussed separately. (See "Evaluation of acute pharyngitis in adults" and "Group A streptococcal tonsillopharyngitis in children and adolescents: Clinical features and diagnosis".)

A persistent, severe sore throat accompanied by fever, trismus, or a muffled voice suggests a local complication such as peritonsillar cellulitis or abscess. These diagnoses are discussed separately. (See "Complications of streptococcal tonsillopharyngitis" and "Peritonsillar cellulitis and abscess".)

Antibiotic treatment — We generally repeat a 10-day course of antibiotic treatment for patients with persistent or recurrent streptococcal pharyngitis. The selection of an antibiotic varies based on patient history (table 1).

For patients who were nonadherent to the initial antibiotic regimen, we typically treat with intramuscular penicillin. Injections of penicillin G benzathine provide bactericidal levels against GAS for 21 to 28 days. For those who are allergic or who cannot otherwise tolerate penicillin, we individualize antibiotic selection based on the patient's preferences and reasons for nonadherence.

For patients with persistent infection or an initial recurrence, we usually select an antibiotic that has greater beta-lactamase stability than the one used for the initial treatment course. As examples, if penicillin was used for initial treatment, we use either amoxicillin-clavulanate or a first-generation cephalosporin; if a first-generation cephalosporin was used, we select a later-generation cephalosporin (table 6).

The approach is based on a meta-analyses of four randomized trials evaluating over 1300 adults and children with GAS pharyngitis that showed decreased clinical relapse rates when comparing cephalosporins with penicillins (25 versus 46 percent; odds ratio 0.55, 95% CI 0.30-0.99) [66]. Additional studies suggest that bacteriologic cure rates may be higher for cephalosporins compared with penicillin [67-70]. Scientific observations also support the selection of antibiotics with beta-lactamase stability when treating persistent or recurrent GAS infection [71-73]. Some bacteria that colonize the oropharynx, such as Staphylococcus aureus, Haemophilus influenza, and Moraxella catarrhalis, produce beta-lactamases that inactivate penicillin, leading to decreased activity of penicillin against GAS [74-76]. Penicillin also decreases the quantity of alpha-streptococci in the oropharynx, which naturally protect against GAS infection [77-79]. Cumulatively, these effects may inadvertently promote the survival and persistence of GAS in the oropharynx. By contrast, antibiotics with beta-lactamase activity may have a more balanced effect on the oropharyngeal flora, resulting in greater likelihood of GAS eradication.

A small number of patients experience multiple recurrences, which may be related to the infecting GAS strain [80-82], host immune response [58,83], or other factors that are not yet well characterized.

For patients with multiple recurrences of GAS pharyngitis, we attempt treatment with an antibiotic from a class that has not been used previously, such as clindamycin.

For patients with frequent, mild to moderate recurrent infections, delaying the start of antibiotic therapy by two to three days is an alternate approach. This approach is derived from observational data that suggest delaying therapy may allow the development of immunity against the infecting strain, resulting in higher eradication rates [58,64,83] without increasing the risk of acute rheumatic fever [84,85]. We generally avoid this approach in patients with severe symptoms or when GAS is actively circulating in the community, as it prolongs symptom duration and may increase the risk of suppurative complications and/or transmission of GAS to others.

For patients with frequent, severe episodes of GAS pharyngitis that recur despite appropriate antibiotic treatment, we consider tonsillectomy. (See 'Tonsillectomy' below.)

It is not necessary to perform follow-up testing for persistent or recurrent infection unless the patient becomes symptomatic after antibiotic treatment or special circumstances as outlined above are present. (See 'Indications for test of cure' above.)

When recurrent infections are thought to be due to ongoing GAS circulation among household members, we consider testing all household members and treating those who test positive. When recurrent infections are thought to be due to ongoing GAS circulation in other close-contact settings such as daycare centers or workplaces, we determine the best management approach on a case-by-case basis.

Tonsillectomy — Tonsillectomy is rarely indicated for patients with recurrent GAS pharyngitis. We determine the need for tonsillectomy in each individual case based on the patient age, the frequency and severity of infections, history of antibiotic use, and patient values and preferences.

Detailed indications for tonsillectomy in adults and children with recurrent pharyngitis and supporting evidence are discussed separately. (See "Tonsillectomy and/or adenoidectomy in children: Indications and contraindications", section on 'Recurrent throat infection' and "Tonsillectomy in adults: Indications", section on 'Recurrent and chronic pharyngotonsillitis'.)

PREVENTION

General prevention

Hand hygiene — Hand hygiene is a key measure for preventing spread to others, especially after coughing or sneezing and before preparing foods or eating, and we remind all patients of its importance.

Postexposure prophylaxis — Testing and treatment of asymptomatic persons who have been exposed to a patient with group A Streptococcus (GAS) pharyngitis are not routinely recommended [23], except for patients with a history of acute rheumatic fever, during outbreaks of acute rheumatic fever and/or poststreptococcal glomerulonephritis, or when GAS infections are recurring in households or other close-contact settings.

Special populations

Patients with a history of acute rheumatic fever — Patients with a history of acute rheumatic fever are at high risk for recurrent rheumatic fever and the development of chronic valvular heart disease with any subsequent GAS infection. We educate these patients on the risk of recurrence and its complications and recommend long-term antibiotic prophylaxis. Antibiotic selection and duration of therapy vary based on patient characteristics and medication availability (table 7 and table 8).

Details on acute rheumatic fever, rheumatic heart disease, and their prevention are discussed separately. (See "Acute rheumatic fever: Clinical manifestations and diagnosis" and "Acute rheumatic fever: Treatment and prevention" and "Clinical manifestations and diagnosis of rheumatic heart disease" and "Management and prevention of rheumatic heart disease".)

Chronic GAS carriers — Antibiotic treatment is not routinely recommended for chronic carriers [23]. Carriers are unlikely to transmit group A Streptococcus (GAS) to others [62,86,87] and are at very low risk for developing suppurative complications or acute rheumatic fever [10]. However, we do consider treating carriers during outbreaks of acute rheumatic fever and/or poststreptococcal glomerulonephritis or when GAS infections are recurring in households or other close-contact settings.

Oral options for treatment of chronic carriage include clindamycin, amoxicillin-clavulanate, and penicillin plus rifampin; the duration of treatment is usually 10 days [23]. When used with either oral or parenteral penicillin, rifampin is typically given only during the last four days of therapy.

Prevention of foodborne illness — Streptococcal contamination of food has been implicated in foodborne outbreaks of pharyngitis [88-92], and foodborne transmission of GAS pharyngitis by asymptomatic food service workers with nasopharyngeal carriage has been reported [91,93,94]. Factors that can reduce foodborne transmission of GAS pharyngitis include thorough cooking, complete reheating, and use of gloves while handling food [88,95].

Vaccination — No vaccine against GAS is available for clinical use. However, research on GAS vaccine development is ongoing [96-100]. An important area of uncertainty is whether vaccine-induced antibodies may cross-react with host tissue to produce nonsuppurative sequelae in the absence of clinical infection.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Streptococcal tonsillopharyngitis".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topics (see "Patient education: Strep throat in adults (The Basics)" and "Patient education: Strep throat in children (The Basics)" and "Patient education: Scarlet fever (The Basics)")

Beyond the Basics topics (see "Patient education: Sore throat in children (Beyond the Basics)" and "Patient education: Sore throat in adults (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

Importance of treatment – Group A Streptococcus (GAS), or Streptococcus pyogenes, is the leading bacterial cause of tonsillopharyngitis in adults and children worldwide. GAS is one of the few causes of tonsillopharyngitis or pharyngitis for which antibiotic treatment is recommended. (See 'Introduction' above.)

The goals of antibiotic therapy for GAS pharyngitis include symptom relief, preventing complications, and preventing transmission to others. (See 'Goals of treatment' above.)

Treatment recommendations

Whom to treat – We recommend antibiotic treatment for any patient with symptomatic pharyngitis or tonsillopharyngitis who has a positive microbiologic test (ie, nucleic acid amplification test [NAAT], rapid antigen test, or culture) for GAS (Grade 1A). We generally do not treat patients who do not have microbiologic confirmation of infection or who are chronic carriers. (See 'Whom to treat' above.)

Preferred treatment for adults – For most adults, we treat with oral penicillin V 500 mg two to three times daily for a total of 10 days. Penicillin is the treatment of choice for GAS pharyngitis due to its efficacy, safety, narrow spectrum, and low cost (table 1 and algorithm 2). (See 'Antibiotic treatment' above.)

Preferred treatment for children – For most children, we use either oral penicillin V or amoxicillin. For young children, amoxicillin is often preferred because the taste of the amoxicillin suspension is more palatable than that of penicillin (table 2 and algorithm 2). (See 'Antibiotic treatment' above.)

Treatment for patients with a history of acute rheumatic fever – For patients with a history of acute rheumatic fever who are not receiving antibiotic prophylaxis, we select among oral penicillin V, oral amoxicillin, or a single dose of intramuscular penicillin G benzathine. The choice is based on drug availability, cost, likelihood of adherence with oral therapy, and patient values and preferences (table 1 and table 2 and algorithm 2). (See 'Antibiotic treatment' above.)

Alternatives for patients who cannot tolerate penicillin – For patients who are allergic to or who cannot tolerate penicillin, alternatives include cephalosporins, clindamycin, and macrolides. Selection among these agents is based on the nature of the drug allergy or intolerance and local antibiotic resistance rates (table 3 and table 1 and table 2 and algorithm 2). (See 'Alternatives to penicillin' above.)

Symptom resolution and return to work – Fever and sore throat typically resolve within one to three days. Most patients can return to work, school, or daycare after 12 to 24 hours of antibiotic therapy, provided they are afebrile and otherwise well. (See 'Resolution of symptoms' above.)

A test of cure is usually not needed for patients who are asymptomatic at the end of a course of antibiotic therapy, except for those with a history of acute rheumatic fever or in other special circumstances. (See 'Indications for test of cure' above.)

Management of persistent symptoms after a course of antibiotics – For patients who have persistent or recurrent symptoms after completing a course of antibiotic therapy, we repeat microbiologic testing when symptoms are compatible with GAS infection. Because chronic GAS carriage can occur after antibiotic therapy, we generally avoid testing in patients who have symptoms that are more compatible with viral pharyngitis or other etiology. (See 'Persistent or recurrent symptoms' above.)

For patients with microbiologically proven recurrent or persistent GAS pharyngitis, we repeat a 10-day course of antibiotic therapy (Grade 2C) and generally select an antibiotic that has greater beta-lactamase stability than the one used initially. Tonsillectomy is rarely indicated for such patients. (See 'Antibiotic treatment' above and 'Tonsillectomy' above.)

Prophylaxis for patients with a history of acute rheumatic fever – Antibiotic prophylaxis is used for patients with a history of acute rheumatic fever because these patients are at high risk for recurrence and for the development of chronic valvular heart disease. Antibiotic prophylaxis is not recommended for chronic carriers, except in special circumstances. (See 'Prevention' above.)

  1. Efstratiou A, Lamagni T. Epidemiology of Streptococcus pyogenes. In: Streptococcus pyogenes: Basic Biology to Clinical Manifestations, Ferretti JJ, Stevens DL, Fischetti VA (Eds), University of Oklahoma Health Sciences Center, Oklahoma City 2016.
  2. Gunnarsson RK, Holm SE, Söderström M. The prevalence of beta-haemolytic streptococci in throat specimens from healthy children and adults. Implications for the clinical value of throat cultures. Scand J Prim Health Care 1997; 15:149.
  3. Schwartz RH, Wientzen RL Jr, Pedreira F, et al. Penicillin V for group A streptococcal pharyngotonsillitis. A randomized trial of seven vs ten days' therapy. JAMA 1981; 246:1790.
  4. Pontin IP, Sanchez DC, Di Francesco R. Asymptomatic Group A Streptococcus carriage in children with recurrent tonsillitis and tonsillar hypertrophy. Int J Pediatr Otorhinolaryngol 2016; 86:57.
  5. Abdissa A, Asrat D, Kronvall G, et al. Throat carriage rate and antimicrobial susceptibility pattern of group A Streptococci (GAS) in healthy Ethiopian school children. Ethiop Med J 2011; 49:125.
  6. Nayiga I, Okello E, Lwabi P, Ndeezi G. Prevalence of group a streptococcus pharyngeal carriage and clinical manifestations in school children aged 5-15 yrs in Wakiso District, Uganda. BMC Infect Dis 2017; 17:248.
  7. Marshall HS, Richmond P, Nissen M, et al. Group A Streptococcal Carriage and Seroepidemiology in Children up to 10 Years of Age in Australia. Pediatr Infect Dis J 2015; 34:831.
  8. Martin JM, Green M, Barbadora KA, Wald ER. Group A streptococci among school-aged children: clinical characteristics and the carrier state. Pediatrics 2004; 114:1212.
  9. Shaikh N, Leonard E, Martin JM. Prevalence of streptococcal pharyngitis and streptococcal carriage in children: a meta-analysis. Pediatrics 2010; 126:e557.
  10. Kaplan EL. The group A streptococcal upper respiratory tract carrier state: an enigma. J Pediatr 1980; 97:337.
  11. Spinks A, Glasziou PP, Del Mar CB. Antibiotics for sore throat. Cochrane Database Syst Rev 2013; :CD000023.
  12. Little P, Hobbs FD, Moore M, et al. Clinical score and rapid antigen detection test to guide antibiotic use for sore throats: randomised controlled trial of PRISM (primary care streptococcal management). BMJ 2013; 347:f5806.
  13. BRINK WR, RAMMELKAMP CH Jr, DENNY FW, WANNAMAKER LW. Effect in penicillin and aureomycin on the natural course of streptococcal tonsillitis and pharyngitis. Am J Med 1951; 10:300.
  14. Roth GA, Huffman MD, Moran AE, et al. Global and regional patterns in cardiovascular mortality from 1990 to 2013. Circulation 2015; 132:1667.
  15. Carapetis JR, Steer AC, Mulholland EK, Weber M. The global burden of group A streptococcal diseases. Lancet Infect Dis 2005; 5:685.
  16. Beaudoin A, Edison L, Introcaso CE, et al. Acute rheumatic fever and rheumatic heart disease among children--American Samoa, 2011-2012. MMWR Morb Mortal Wkly Rep 2015; 64:555.
  17. Brundage JF, Gunzenhauser JD, Longfield JN, et al. Epidemiology and control of acute respiratory diseases with emphasis on group A beta-hemolytic streptococcus: a decade of U.S. Army experience. Pediatrics 1996; 97:964.
  18. BREESE BB, DISNEY FA. Factors influencing the spread of beta hemolytic streptococcal infections within the family group. Pediatrics 1956; 17:834.
  19. Lamagni TL, Oliver I, Stuart JM. Global assessment of invasive group a streptococcus infection risk in household contacts. Clin Infect Dis 2015; 60:166.
  20. Snellman LW, Stang HJ, Stang JM, et al. Duration of positive throat cultures for group A streptococci after initiation of antibiotic therapy. Pediatrics 1993; 91:1166.
  21. Schwartz RH, Kim D, Martin M, Pichichero ME. A Reappraisal of the Minimum Duration of Antibiotic Treatment Before Approval of Return to School for Children With Streptococcal Pharyngitis. Pediatr Infect Dis J 2015; 34:1302.
  22. WANNAMAKER LW, RAMMELKAMP CH Jr, DENNY FW, et al. Prophylaxis of acute rheumatic fever by treatment of the preceding streptococcal infection with various amounts of depot penicillin. Am J Med 1951; 10:673.
  23. Shulman ST, Bisno AL, Clegg HW, et al. Clinical practice guideline for the diagnosis and management of group A streptococcal pharyngitis: 2012 update by the Infectious Diseases Society of America. Clin Infect Dis 2012; 55:1279.
  24. Harris AM, Hicks LA, Qaseem A, High Value Care Task Force of the American College of Physicians and for the Centers for Disease Control and Prevention. Appropriate Antibiotic Use for Acute Respiratory Tract Infection in Adults: Advice for High-Value Care From the American College of Physicians and the Centers for Disease Control and Prevention. Ann Intern Med 2016; 164:425.
  25. Tanz RR, Gewitz MH, Kaplan EL, Shulman ST. Stay the Course: Targeted Evaluation, Accurate Diagnosis, and Treatment of Streptococcal Pharyngitis Prevent Acute Rheumatic Fever. J Pediatr 2020; 216:208.
  26. Gerber MA, Baltimore RS, Eaton CB, et al. Prevention of rheumatic fever and diagnosis and treatment of acute Streptococcal pharyngitis: a scientific statement from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee of the Council on Cardiovascular Disease in the Young, the Interdisciplinary Council on Functional Genomics and Translational Biology, and the Interdisciplinary Council on Quality of Care and Outcomes Research: endorsed by the American Academy of Pediatrics. Circulation 2009; 119:1541.
  27. Nishimura RA, Otto CM, Bonow RO, et al. 2014 AHA/ACC guideline for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Thorac Cardiovasc Surg 2014; 148:e1.
  28. American Academy of Pediatrics. Group A Streptococcus. In: Red Book: 2015 Report of the Committee of Infectious Diseases, 30th, Kimberlin DW, Brady MT, Jackson MA, Long SS (Eds), American Academy of Pediatrics, Elk Grove Village, IL 2018. p.732.
  29. ESCMID Sore Throat Guideline Group, Pelucchi C, Grigoryan L, et al. Guideline for the management of acute sore throat. Clin Microbiol Infect 2012; 18 Suppl 1:1.
  30. The Australian guideline for prevention, diagnosis and management of acute rheumatic fever and rheumatic heart disease (2nd edition) https://www.rhdaustralia.org.au/sites/default/files/resources/guideline_0_0.pdf (Accessed on October 27, 2017).
  31. New Zealand Guidelines for Rheumatic Fever. Group A Streptococcal Sore Throat Management Guideline: 2014 Update http://assets.heartfoundation.org.nz/shop/heart-healthcare/non-stock-resources/gas-sore-throat-rheumatic-fever-guideline.pdf (Accessed on October 27, 2017).
  32. Gopichand I, Williams GD, Medendorp SV, et al. Randomized, single-blinded comparative study of the efficacy of amoxicillin (40 mg/kg/day) versus standard-dose penicillin V in the treatment of group A streptococcal pharyngitis in children. Clin Pediatr (Phila) 1998; 37:341.
  33. Curtin-Wirt C, Casey JR, Murray PC, et al. Efficacy of penicillin vs. amoxicillin in children with group A beta hemolytic streptococcal tonsillopharyngitis. Clin Pediatr (Phila) 2003; 42:219.
  34. Lennon DR, Farrell E, Martin DR, Stewart JM. Once-daily amoxicillin versus twice-daily penicillin V in group A beta-haemolytic streptococcal pharyngitis. Arch Dis Child 2008; 93:474.
  35. Feder HM Jr, Gerber MA, Randolph MF, et al. Once-daily therapy for streptococcal pharyngitis with amoxicillin. Pediatrics 1999; 103:47.
  36. Clegg HW, Ryan AG, Dallas SD, et al. Treatment of streptococcal pharyngitis with once-daily compared with twice-daily amoxicillin: a noninferiority trial. Pediatr Infect Dis J 2006; 25:761.
  37. Kaplan EL, Gooch III WM, Notario GF, Craft JC. Macrolide therapy of group A streptococcal pharyngitis: 10 days of macrolide therapy (clarithromycin) is more effective in streptococcal eradication than 5 days (azithromycin). Clin Infect Dis 2001; 32:1798.
  38. Altamimi S, Khalil A, Khalaiwi KA, et al. Short-term late-generation antibiotics versus longer term penicillin for acute streptococcal pharyngitis in children. Cochrane Database Syst Rev 2012; :CD004872.
  39. WANNAMAKER LW, DENNY FW, PERRY WD, et al. The effect of penicillin prophylaxis on streptococcal disease rates and the carrier state. N Engl J Med 1953; 249:1.
  40. Gerber MA, Randolph MF, Chanatry J, et al. Five vs ten days of penicillin V therapy for streptococcal pharyngitis. Am J Dis Child 1987; 141:224.
  41. Falagas ME, Vouloumanou EK, Matthaiou DK, et al. Effectiveness and safety of short-course vs long-course antibiotic therapy for group a beta hemolytic streptococcal tonsillopharyngitis: a meta-analysis of randomized trials. Mayo Clin Proc 2008; 83:880.
  42. Skoog Ståhlgren G, Tyrstrup M, Edlund C, et al. Penicillin V four times daily for five days versus three times daily for 10 days in patients with pharyngotonsillitis caused by group A streptococci: randomised controlled, open label, non-inferiority study. BMJ 2019; 367:l5337.
  43. BREESE BB, DISNEY FA. Penicillin in the treatment of streptococcal infections; a comparison of effectiveness of five different oral and one parenteral form. N Engl J Med 1958; 259:57.
  44. Tack KJ, Henry DC, Gooch WM, et al. Five-day cefdinir treatment for streptococcal pharyngitis. Cefdinir Pharyngitis Study Group. Antimicrob Agents Chemother 1998; 42:1073.
  45. Pichichero ME, Gooch WM 3rd. Comparison of cefdinir and penicillin V in the treatment of pediatric streptococcal tonsillopharyngitis. Pediatr Infect Dis J 2000; 19:S171.
  46. Pichichero ME, Gooch WM, Rodriguez W, et al. Effective short-course treatment of acute group A beta-hemolytic streptococcal tonsillopharyngitis. Ten days of penicillin V vs 5 days or 10 days of cefpodoxime therapy in children. Arch Pediatr Adolesc Med 1994; 148:1053.
  47. Tack KJ, Hedrick JA, Rothstein E, et al. A study of 5-day cefdinir treatment for streptococcal pharyngitis in children. Cefdinir Pediatric Pharyngitis Study Group. Arch Pediatr Adolesc Med 1997; 151:45.
  48. Casey JR, Pichichero ME. Higher dosages of azithromycin are more effective in treatment of group A streptococcal tonsillopharyngitis. Clin Infect Dis 2005; 40:1748.
  49. Richter SS, Heilmann KP, Beekmann SE, et al. Macrolide-resistant Streptococcus pyogenes in the United States, 2002-2003. Clin Infect Dis 2005; 41:599.
  50. Lin JN, Chang LL, Lai CH, et al. High prevalence of fluoroquinolone-nonsusceptible Streptococcus pyogenes emm12 in Taiwan. Diagn Microbiol Infect Dis 2015; 83:187.
  51. Petrelli D, Di Luca MC, Prenna M, et al. Characterization of levofloxacin non-susceptible clinical Streptococcus pyogenes isolated in the central part of Italy. Eur J Clin Microbiol Infect Dis 2014; 33:241.
  52. Van Heirstraeten L, Leten G, Lammens C, et al. Increase in fluoroquinolone non-susceptibility among clinical Streptococcus pyogenes in Belgium during 2007-10. J Antimicrob Chemother 2012; 67:2602.
  53. Palmieri C, Vecchi M, Littauer P, et al. Clonal spread of macrolide- and tetracycline-resistant [erm(A) tet(O)] emm77 Streptococcus pyogenes isolates in Italy and Norway. Antimicrob Agents Chemother 2006; 50:4229.
  54. Michos AG, Bakoula CG, Braoudaki M, et al. Macrolide resistance in Streptococcus pyogenes: prevalence, resistance determinants, and emm types. Diagn Microbiol Infect Dis 2009; 64:295.
  55. van Driel ML, De Sutter AI, Thorning S, Christiaens T. Different antibiotic treatments for group A streptococcal pharyngitis. Cochrane Database Syst Rev 2021; 3:CD004406.
  56. US Food and Drug Administration. FDA Drug Safety Communication; May 12, 2016 https://www.fda.gov/Drugs/DrugSafety/ucm511530.htm (Accessed on September 11, 2017).
  57. Randolph MF, Gerber MA, DeMeo KK, Wright L. Effect of antibiotic therapy on the clinical course of streptococcal pharyngitis. J Pediatr 1985; 106:870.
  58. Pichichero ME, Disney FA, Talpey WB, et al. Adverse and beneficial effects of immediate treatment of Group A beta-hemolytic streptococcal pharyngitis with penicillin. Pediatr Infect Dis J 1987; 6:635.
  59. Krober MS, Bass JW, Michels GN. Streptococcal pharyngitis. Placebo-controlled double-blind evaluation of clinical response to penicillin therapy. JAMA 1985; 253:1271.
  60. Del Mar CB, Glasziou PP, Spinks AB. Antibiotics for sore throat. Cochrane Database Syst Rev 2000; :CD000023.
  61. Gilbert GG, Pruitt BE. School health education in the United States. Hygie 1984; 3:10.
  62. Kaplan EL, Gastanaduy AS, Huwe BB. The role of the carrier in treatment failures after antibiotic for group A streptococci in the upper respiratory tract. J Lab Clin Med 1981; 98:326.
  63. Woodin KA, Lee LH, Pichichero ME. Milder symptoms occur in recurrent episodes of streptococcal infection. Am J Dis Child 1991; 145:389.
  64. Pichichero ME, Hoeger W, Marsocci SM, et al. Variables influencing penicillin treatment outcome in streptococcal tonsillopharyngitis. Arch Pediatr Adolesc Med 1999; 153:565.
  65. Cohen JF, Bertille N, Cohen R, Chalumeau M. Rapid antigen detection test for group A streptococcus in children with pharyngitis. Cochrane Database Syst Rev 2016; 7:CD010502.
  66. van Driel ML, De Sutter AI, Habraken H, et al. Different antibiotic treatments for group A streptococcal pharyngitis. Cochrane Database Syst Rev 2016; 9:CD004406.
  67. Yildirim I, Ceyhan M, Gür D, Kaymakoğlu I. Comparison of the effect of benzathine penicillin G, clarithromycin, cefprozil and amoxicillin/clavulanate on the bacteriological response and throat flora in group A beta hemolytic streptococcal tonsillopharyngitis. Turk J Pediatr 2008; 50:120.
  68. Brook I, Gober AE. Failure to eradicate streptococci and beta-lactamase producing bacteria. Acta Paediatr 2008; 97:193.
  69. Casey JR, Pichichero ME. Symptomatic relapse of group A beta-hemolytic streptococcal tonsillopharyngitis in children. Clin Pediatr (Phila) 2007; 46:307.
  70. Brook I, Gober AE. Recovery of interfering and beta-lactamase-producing bacteria from group A beta-haemolytic streptococci carriers and non-carriers. J Med Microbiol 2006; 55:1741.
  71. Gaffney RJ, Freeman DJ, Walsh MA, Cafferkey MT. Differences in tonsil core bacteriology in adults and children: a prospective study of 262 patients. Respir Med 1991; 85:383.
  72. Lund B, Edlund C, Rynnel-Dagöö B, et al. Ecological effects on the oro- and nasopharyngeal microflora in children after treatment of acute otitis media with cefuroxime axetil or amoxycillin-clavulanate as suspensions. Clin Microbiol Infect 2001; 7:230.
  73. Lafontaine ER, Wall D, Vanlerberg SL, et al. Moraxella catarrhalis coaggregates with Streptococcus pyogenes and modulates interactions of S. pyogenes with human epithelial cells. Infect Immun 2004; 72:6689.
  74. Gaffney RJ, Cafferkey MT. Bacteriology of normal and diseased tonsils assessed by fine-needle aspiration: Haemophilus influenzae and the pathogenesis of recurrent acute tonsillitis. Clin Otolaryngol Allied Sci 1998; 23:181.
  75. Brook I, Yocum P, Foote PA Jr. Changes in the core tonsillar bacteriology of recurrent tonsillitis: 1977-1993. Clin Infect Dis 1995; 21:171.
  76. Brook I. Overcoming penicillin failures in the treatment of Group A streptococcal pharyngo-tonsillitis. Int J Pediatr Otorhinolaryngol 2007; 71:1501.
  77. Falck G, Grahn-Håkansson E, Holm SE, et al. Tolerance and efficacy of interfering alpha-streptococci in recurrence of streptococcal pharyngotonsillitis: a placebo-controlled study. Acta Otolaryngol 1999; 119:944.
  78. Roos K, Holm SE, Grahn-Håkansson E, Lagergren L. Recolonization with selected alpha-streptococci for prophylaxis of recurrent streptococcal pharyngotonsillitis--a randomized placebo-controlled multicentre study. Scand J Infect Dis 1996; 28:459.
  79. Roos K, Holm SE, Grahn E, Lind L. Alpha-streptococci as supplementary treatment of recurrent streptococcal tonsillitis: a randomized placebo-controlled study. Scand J Infect Dis 1993; 25:31.
  80. Wozniak A, Scioscia N, Geoffroy E, et al. Importance of adhesins in the recurrence of pharyngeal infections caused by Streptococcus pyogenes. J Med Microbiol 2017; 66:517.
  81. Ogawa T, Terao Y, Okuni H, et al. Biofilm formation or internalization into epithelial cells enable Streptococcus pyogenes to evade antibiotic eradication in patients with pharyngitis. Microb Pathog 2011; 51:58.
  82. Podbielski A, Beckert S, Schattke R, et al. Epidemiology and virulence gene expression of intracellular group A streptococci in tonsils of recurrently infected adults. Int J Med Microbiol 2003; 293:179.
  83. el-Daher NT, Hijazi SS, Rawashdeh NM, et al. Immediate vs. delayed treatment of group A beta-hemolytic streptococcal pharyngitis with penicillin V. Pediatr Infect Dis J 1991; 10:126.
  84. CATANZARO FJ, STETSON CA, MORRIS AJ, et al. The role of the streptococcus in the pathogenesis of rheumatic fever. Am J Med 1954; 17:749.
  85. BROCK LL, SIEGEL AC. Studies on the prevention of rheumatic fever; the effect of time of initiation of treatment of streptococcal infections on the immune response of the host. J Clin Invest 1953; 32:630.
  86. Davies HD, McGeer A, Schwartz B, et al. Invasive group A streptococcal infections in Ontario, Canada. Ontario Group A Streptococcal Study Group. N Engl J Med 1996; 335:547.
  87. KRAUSE RM, RAMMELKAMP CH Jr, DENNY FW Jr, WANNAMAKER LW. Studies of the carrier state following infection with group A streptococci. 1. Effect of climate. J Clin Invest 1962; 41:568.
  88. Kemble SK, Westbrook A, Lynfield R, et al. Foodborne outbreak of group a streptococcus pharyngitis associated with a high school dance team banquet--Minnesota, 2012. Clin Infect Dis 2013; 57:648.
  89. Levy M, Johnson CG, Kraa E. Tonsillopharyngitis caused by foodborne group A streptococcus: a prison-based outbreak. Clin Infect Dis 2003; 36:175.
  90. Katzenell U, Shemer J, Bar-Dayan Y. Streptococcal contamination of food: an unusual cause of epidemic pharyngitis. Epidemiol Infect 2001; 127:179.
  91. Decker MD, Lavely GB, Hutcheson RH Jr, Schaffner W. Food-borne streptococcal pharyngitis in a hospital pediatrics clinic. JAMA 1985; 253:679.
  92. Todd EC, Greig JD, Michaels BS, et al. Outbreaks where food workers have been implicated in the spread of foodborne disease. Part 11. Use of antiseptics and sanitizers in community settings and issues of hand hygiene compliance in health care and food industries. J Food Prot 2010; 73:2306.
  93. Sarvghad MR, Naderi HR, Naderi-Nassab M, et al. An outbreak of food-borne group A Streptococcus (GAS) tonsillopharyngitis among residents of a dormitory. Scand J Infect Dis 2005; 37:647.
  94. McCormick JB, Hayes P, Feldman R. Epidemic streptococcal sore throat following a community picnic. JAMA 1976; 236:1039.
  95. Kaplan EL. Editorial commentary: The epidemiology of group a streptococci: a need to understand the significance of the fertile fields. Clin Infect Dis 2012; 55:488.
  96. Nordström T, Pandey M, Calcutt A, et al. Enhancing Vaccine Efficacy by Engineering a Complex Synthetic Peptide To Become a Super Immunogen. J Immunol 2017; 199:2794.
  97. Burlet E, HogenEsch H, Dunham A, Morefield G. Evaluation of the Potency, Neutralizing Antibody Response, and Stability of a Recombinant Fusion Protein Vaccine for Streptococcus pyogenes. AAPS J 2017; 19:875.
  98. Williamson DA, Smeesters PR, Steer AC, et al. Comparative M-protein analysis of Streptococcus pyogenes from pharyngitis and skin infections in New Zealand: Implications for vaccine development. BMC Infect Dis 2016; 16:561.
  99. Good MF, Pandey M, Batzloff MR, Tyrrell GJ. Strategic development of the conserved region of the M protein and other candidates as vaccines to prevent infection with group A streptococci. Expert Rev Vaccines 2015; 14:1459.
  100. Lewnard JA, King LM, Fleming-Dutra KE, et al. Incidence of Pharyngitis, Sinusitis, Acute Otitis Media, and Outpatient Antibiotic Prescribing Preventable by Vaccination Against Group A Streptococcus in the United States. Clin Infect Dis 2021; 73:e47.
Topic 8049 Version 94.0

References

آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟